Research published today found that the investigational drug patiromer decreased high potassium levels and maintained normal potassium levels in patients with chronic kidney disease in a Phase 3 study. The results of the multicenter trial appear today (November 21, 2014) in an open-access article in the New England Journal of Medicine. This article is accompanied by a second open-access article on Phase 3 results for another anti-hyperkalemia drug (ZS-9), as well as by an open-access editorial entitled, “A New Era for the Treatment of Hyperkalemia?” Elevated potassium, a condition called hyperkalemia, increases the risk of death in high-risk patients and limits the use of several types of drugs, called RAAS (renin-angiotensin-aldosterone system) inhibitors, commonly used to control hypertension and cardiovascular disease and to prevent kidney disorders. "Patients with advanced kidney disease are at highest risk for hyperkalemia thanks to a double whammy," says the study's principal investigator, Matthew R. Weir, M.D., Professor of Medicine and Director of the Division of Nephrology at the University of Maryland School of Medicine. "Their kidneys are unable to remove potassium from the body effectively, and the patient may also be taking certain blood pressure control drugs that have been linked to high potassium levels. Current medications for hyperkalemia have gastrointestinal side effects that limit their extended use. We hoped the drug in this study would do the job with minimal side effects." In this Phase 3 study of 237 patients with chronic kidney disease who were receiving RAAS inhibitors, 76 percent of the patients reached the target potassium level after four weeks on patiromer.

One of the most aggressive and common forms of liver cancer is hepatocellular carcinoma. A team of researchers from the Institute of Cancer Research at the Medical University of Vienna (MedUni Vienna) has now identified the crucial factor involved in the development and progression of this malignant type of tumor: namely, the AXL receptor, which supports cancer-promoting processes and slows down cancer-inhibiting factors. This key finding could make a targeted therapeutic approach possible in future. In the Western world, metabolic diseases and infections with hepatitis C are the most common causes of hepatocellular carcinoma (HCC). The team led by Dr. Wolfgang Mikulits, Head of the Tumor Progression and Metastasis Research Group at the MedUni Vienna Institute of Cancer Research (ICR) and member of the Comprehensive Cancer Center (CCC) Vienna, investigated the role of the AXL receptor tyrosine kinase in the context of liver cancer as part of a study. Says Dr. Mikulits: "Until now, the function of AXL had been barely investigated at all, which is astonishing since this receptor is shown to have been activated in more than 50 per cent of all HCC patients." The researchers were able to demonstrate that the expression and activation of AXL lead to a diversion of signaling pathways, enabling the migration and metastasis of liver cancer cells. As a result, AXL, after binding a 14-3-3 adapter protein, is able to influence the extremely important transforming growth factor beta (TGF-beta) signaling pathway in such a way that it only causes the invasion and metastasis of HCC cells. In contrast to this, AXL inhibits the anti-oncogenic function of TGF-beta. AXL is therefore the crucial factor in the aggressive development of hepatocellular carcinoma.